1. Field of Invention
The invention relates to a modified polymeric shaped body, a method for producing the same and the use thereof.
2. Description of Related Art
AGEs (advanced glycation endproducts) are present in blood and blood plasma, particularly in kidney patients and diabetics. They are proteins that have lost their function as a result of modification and cross-linking with degradation products of sugars. AGEs give rise to various secondary diseases such as arteriosclerosis and amyloidosis. Much research has therefore been carried out on the removal of AGEs from blood or plasma.
Conventional methods of treating blood like high-flux or low-flux dialysis or hemodiafiltration do not bring about an appreciable reduction in AGE concentration.
Various approaches have been suggested in the prior art for removal of AGEs.
The International Journal of Artificial Organs (1993), vol 16, pp. 823-829 describes an adsorber column filled with hydrophobised cellulose spheres.
While this was successful in reducing the concentration of β2 microglobulin, and therefore also of AGE-modified β2 microglobulin, it also simultaneously removed other proteins, such as RBP, prolactin, C-PTH, HS-PTH and WBC, that should not be removed.
U.S. Pat. No. 5,891,341 describes a cysteine-bounded loop consisting of 17-18 aminoacids that is immobilised on a dialysis membrane. This allows the removal of various AGEs from the blood during dialysis. However, only those AGEs dissolved in the blood are removed; AGEs that have already been deposited are not affected by this treatment. Moreover, the handling of a protein-modified membrane of this type is considerably complicated by the fact that it cannot be sterilised. In addition, AGE formation as such is not prevented.
U.S. Pat. No. 5,128,360 discloses that compounds with active nitrogen such as aminoguanidine, α-hydrazinohistidine and lysine or mixtures thereof are agents for inhibition of AGE formation. According to U.S. Pat. No. 5,128,360, these compounds appear to react with early glycosylation products, which are then prevented from forming AGEs. The compounds are administered as drugs and therefore necessarily come into contact with tissue.
The journal Endocrinology and Metabolism (1996), vol 3, pp 149-166 discloses that aminoguanidine intercepts a-oxyaldehydes such as glyoxal, methylglyoxal and 3-deoxyglueosone, i.e., AGE precursors, thus hindering AGE formation. However, aminoguanidine in contact with tissue leads to highly undesirable side-effects in the form of NO-synthase inhibition.